POCKET GUIDE

TO COPD DIAGNOSIS, MANAGEMENT,

AND PREVENTION
A Guide for Health Care Professionals
UP DATED 2010
Global Initiative for Chronic
Obstructive
Lung
Disease
Global Initiative for Chronic
Obstructive
Lung
Disease
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GOLD Ex ecu t iv e Com mit t ee
Roberto Rodriguez-Roisin, MD, Spain, Chair
Antonio Anzueto, MD, US (representing ATS)
Jean Bourbeau, MD, Canada
Teresita S. DeGuia, MD, Philippines
David Hui, MD, Hong Kong, ROC
Christine Jenkins, MD, Australia
Fernando Martinez, MD, US
Mara Montes de Oca, MD, PhD (representing ALAT)
Chris van Weel, MD, Netherlands (representing WONCA)
Jorgen Vestbo, MD, Denmark
Obser v er :
Jadwiga Wedzicha, MD, UK (Representing ERS)
GOLD Nat ional L eader s
Representatives from many countries serve as a network for the dissemination and
implementation of programs for diagnosis, management, and prevention of COPD.
The GOLD Executive Committee is grateful to the many GOLD National Leaders who
participated in discussions of concepts that appear in GOLD reports, and for their
comments during the review of the 2006 Global Strategy for the Diagnosis,
Management, and Prevention of COPD.
Global Initiative for Chronic
Obstructive
Lung
Disease
Pocket Guide to COPD Diagnosis, Management,
and Prevention
2010 Global Initiative for Chronic Obstructive Lung Disease, Inc.
Michiaki Mishima, MD, Japan (representing APSR)
Robert Stockley, MD, UK
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TABL E OF CONTENTS
PREFACE
KEY POI NTS
WHAT I S CHRONI C OBSTRUCTI VE
P ULMONARY DI SEASE (COPD)?
RI SK FACTORS: WHAT CAUSES COPD?
DI AGNOSI NG COPD
Figure 1: Key Indicators for Considering a
COPD Diagnosis
Figure 2: Normal Spirogram and Spirogram Typical of
Patients with Mild to Moderate COPD
Figure 3: Differential Diagnosis of COPD
COMP ONENTS OF CARE:
A COP D MANAGEMENT PROGRAM
Com ponent 1: Ass es s and Monit or Disease
Com ponent 2: Redu ce Risk Fact or s
Figure 4: Strategy to Help a Patient Quit Smoking
Com ponent 3: Manage St abl e COP D
Patient Education
Pharmacologic Treatment
Figure 5: Commonly Used Formulations of Drugs for COPD
Non-Pharmacologic Treatment
Figure 6: Therapy at Each Stage of COPD
Com ponent 4: Manage Ex acer bat ions
How to Assess the Severity of an Exacerbation
Home Management
Hospital Management
Figure 7: Indications for Hospital Admission
for Exacerbations
APPENDIX I : SPI ROMETRY FOR DIAGNOSI S OF COPD
3
5
6
7
8
12
13
15
17
22
24
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Chronic Obstructive Pulmonary Disease (COPD) is a major cause of
chronic morbidity and mortality throughout the world. The Gl obal
I nit iat iv e f or Chronic Obst r uct iv e L ung Dis eas e was created to
increase awareness of COPD among health professionals, public health
authorities, and the general public, and to improve prevention and
management through a concerted worldwide effort. The Initiative
prepares scientific reports on COPD, encourages dissemination and
adoption of the reports, and promotes international collaboration on
COPD research.
While COPD has been recognized for many years, public health officials
are concerned about continuing increases in its prevalence and mortality,
which are due in large part to the increasing use of tobacco products
worldwide and the changing age structure of populations in developing
countries. The Gl obal I nit iat iv e f or Chr onic Obst r uct iv e L ung
Dis eas e offers a framework for management of COPD that can be
adapted to local health care systems and resources. Educational tools,
such as laminated cards or computer-based learning programs, can be
prepared that are tailored to these systems and resources.
The Gl obal I nit iat iv e f or Chr onic Obst r uct iv e L ung Dis eas e
program includes the following publications:
Global Strategy for the Diagnosis, Management, and Prevention of
COPD. Scientific information and recommendations for COPD
programs. (Updated 2010)
Executive Summary, Global Strategy for the Diagnosis, Management,
and Prevention of COPD. (Updated 2010)
Pocket Guide to COPD Diagnosis, Management, and Prevention.
Summary of patient care information for primary health care
professionals. (Updated 2010)
What You and Your Family Can Do About COPD. Information booklet
for patients and their families.
PREFACE
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These publications are available on the Internet at www.goldcopd.org.
This site provides links to other websites with information about COPD.
This Pocket Guide has been developed from the Global Strategy for the
Diagnosis, Management, and Prevention of COPD (2010). Technical
discussions of COPD and COPD management, evidence levels, and specific
citations from the scientific literature are included in that source document.
Ack now l edgem ent s: Grateful acknowledgement is given for the educational
grants from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, Dey, Forest
Laboratories, GlaxoSmithKline, Novartis, Nycomed, Pfizer, Philips Respironics, and
Schering-Plough. The generous contributions of these companies assured that the
participants could meet together and publications could be printed for wide distribu-
tion. The participants, however, are solely responsible for the statements and con-
clusions in the publications.
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KEY POINTS
Chr onic Obst r uct iv e P ul m onar y Dis eas e (COP D) is a
preventable and treatable disease with some significant extra-
pulmonary effects that may contribute to the severity in individual
patients. Its pulmonary component is characterized by airflow limitation
that is not fully reversible. The airflow limitation is usually progressive
and associated with an abnormal inflammatory response of the lung
to noxious particles or gases.
Worldwide, the most commonly encountered r is k f act or for COPD
is cigar et t e s mok ing. At ever y poss ibl e oppor t u nit y
indiv idual s w ho s mok e shou l d be encou r aged t o quit . In
many countries, air pollution resulting from the burning of wood and
other biomass fuels has also been identified as a COPD risk factor.
A diagnosis of COPD should be considered in any patient who has
dyspnea, chronic cough or sputum production, and/or a history of
exposure to risk factors for the disease. The diagnosis should be
confirmed by spirometry.
A COPD m anagem ent progr am includes four components:
assess and monitor disease, reduce risk factors, manage stable
COPD, and manage exacerbations.
P har macol ogic t r eat m ent can prevent and control symptoms,
reduce the frequency and severity of exacerbations, improve health
status, and improve exercise tolerance.
P at ient educat ion can help improve skills, ability to cope with
illness, and health status. It is an effective way to accomplish smoking
cessation, initiate discussions and understanding of advance directives
and end-of-life issues, and improve responses to acute exacerbations.
COPD is often associated with ex acer bat ions of symptoms.
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WHAT IS CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
(COPD)?
Chronic Obs t r u ct ive Pu l monar y Disease (COPD) is a preventable
and treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary component
is characterized by airflow limitation that is not fully reversible. The air-
flow limitation is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or gases.
This definition does not use the terms chronic bronchitis and emphysema*
and excludes asthma (reversible airflow limitation).
Sy mpt om s of COPD incl ude:
Cough
Sputum production
Dyspnea on exertion
Episodes of acute worsening of these symptoms often occur.
*Chronic bronchitis, defined as the presence of cough and sputum production for at least 3
months in each of 2 consecutive years, is not necessarily associated with airflow limitation.
Emphysema, defined as destruction of the alveoli, is a pathological term that is sometimes
(incorrectly) used clinically and describes only one of several structural abnormalities present
in patients with COPD.
6
Chronic cou gh and spu t u m pr odu ct ion of t en pr ecede t he
dev el opm ent of air f l ow l imit at ion by m any y ear s, alt hou gh
not al l indiv idu al s w it h cou gh and s pu t u m pr odu ct ion go on
t o dev el op COP D.
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RISK FACTORS:
WHAT CAUSES COPD?
Wor l dw ide, cigar et t e sm ok ing is t he most com m onl y
encount er ed r is k f act or f or COPD.
The genetic risk factor that is best documented is a severe hereditary
deficiency of alpha-1 antitrypsin. It provides a model for how other
genetic risk factors are thought to contribute to COPD.
COPD risk is related to the total burden of inhaled particles a person
encounters over their lifetime:
Tobacco s mok e, including cigarette, pipe, cigar, and other types
of tobacco smoking popular in many countries, as well as
environmental tobacco smoke (ETS)
Occupat ional dust s and chemical s (vapors, irritants, and
fumes) when the exposures are sufficiently intense or prolonged
Indoor air pol l ut ion from biomass fuel used for cooking and
heating in poorly vented dwellings, a risk factor that particularly
affects women in developing countries
Out door air pol l ut ion also contributes to the lungs total burden
of inhaled particles, although it appears to have a relatively small
effect in causing COPD
In addition, any factor that affects lung growth during gestation and
childhood (low birth weight, respiratory infections, etc.) has the potential
for increasing an individuals risk of developing COPD.
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DIAGNOSING
COPD
A diagnosis of COPD should be considered in any patient who has dyspnea,
chronic cough or sputum production, and/or a history of exposure to risk
factors for the disease, especially cigarette smoking (Figur e 1).
The diagnosis s hou l d be conf ir med by spirom et r y *
(Figur e 2, page 9 and Appendix I, page 24).
*Where spirometry is unavailable, the diagnosis of COPD should be made using all
available tools. Clinical symptoms and signs (abnormal shortness of breath and increased
forced expiratory time) can be used to help with the diagnosis. A low peak flow is consistent
with COPD but has poor specificity since it can be caused by other lung diseases and by
poor performance. In the interest of improving the accuracy of a diagnosis of COPD, every
effort should be made to provide access to standardized spirometry.
8
Figu r e 1: Key I ndicat or s f or Cons ider ing a COPD Diagnosis
Consider COPD, and perform spirometry, if any of these indicators
are present in an individual over age 40. These indicators are not
diagnostic themselves, but the presence of multiple key indicators
increases the probability of a diagnosis of COPD.
Dy s pnea that is: Progressive (worsens over time).
Usually worse with exercise.
Persistent (present every day).
Described by the patient as an increased
effort to breathe, heaviness, air hunger,
or gasping.
Chr onic cou gh: May be intermittent and may be unproductive.
Chr onic sput um pr oduct ion:
Any pattern of chronic sputum production may
indicate COPD.
Hist or y of ex posur e t o r isk f act or s:
Tobacco smok e (including popular local
pr epar at ions).
Occupational dusts and chemicals.
Smoke from home cooking and heating fuel.
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When performing spirometry, measure:
Forced Vital Capacity (FVC) and
Forced Expiratory Volume in one second (FEV
1
).
Calculate the FEV
1
/FVC ratio.
Spirometric results are expressed as % Pr edict ed using
appropriate normal values for the persons sex, age, and height.
9
P at ient s w it h COP D t y pical l y s how a decr ease in bot h FEV
1
and FEV
1
/FVC. The degr ee of s pir omet r ic abnor m alit y
gener al l y r ef l ect s t he sev er it y of COP D. How ev er, bot h
s ym pt om s and s pir omet r y s houl d be cons ider ed when
dev el oping an indiv idu al ized m anagem ent st r at egy f or
each pat ient .
Figu r e 2: Nor m al Spir ogr am and Spir ogr am Ty pical of
P at ient s w it h Mil d t o Moder at e COPD*
*Postbronchodilator FEV
1
is recommended for the diagnosis
and assessment of severity of COPD.
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St ages of COP D
St age I : Mil d COPD - Mild airflow limitation (FEV
1
/FVC < 70%;
FEV
1
80% predicted) and sometimes, but not always, chronic cough
and sputum production.
At this stage, the individual may not be aware that his or her lung
function is abnormal.
St age I I : Moder at e COPD - Worsening airflow limitation
(FEV
1
/FVC < 70%; 50% FEV
1
< 80% predicted), with shortness
of breath typically developing on exertion.
This is the stage at which patients typically seek medical attention
because of chronic respiratory symptoms or an exacerbation of their
disease.
St age I I I : Sev er e COPD - Further worsening of airflow limitation
(FEV
1
/FVC < 70%; 30% FEV
1
< 50% predicted), greater shortness of
breath, reduced exercise capacity, and repeated exacerbations which
have an impact on patients quality of life.
St age I V: Ver y Sev er e COPD - Severe airflow limitation
(FEV
1
/FVC < 70%; FEV
1
< 30% predicted) or FEV
1
< 50% predicted
plus chronic respiratory failure. Patients may have Very Severe (Stage IV)
COPD even if the FEV
1
is > 30% predicted, whenever this complication
is present.
At this stage, quality of life is very appreciably impaired and
exacerbations may be life-threatening.
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At Ris k f or COP D
A major objective of GOLD is to increase awareness among health care providers and the
general public of the significance of COPD symptoms. The classification of severity of COPD
now includes four stages classified by spirometryStage I: Mild COPD; Stage II: Moderate
COPD; Stage III: Severe COPD; Stage IV: Very Severe COPD. A fifth categoryStage 0: At
Riskthat appeared in the 2001 report is no longer included as a stage of COPD, as there
is incomplete evidence that the individuals who meet the definition of At Risk (chronic cough
and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD.
Nevertheless, the importance of the public health message that chronic cough and sputum are
not normal is unchanged and their presence should trigger a search for underlying cause(s).
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Dif ferent ial Diagnosis: A major differential diagnosis is asthma. In
some patients with chronic asthma, a clear distinction from COPD is not
possible using current imaging and physiological testing techniques. In these
patients, current management is similar to that of asthma. Other potential
diagnoses are usually easier to distinguish from COPD (Figure 3).
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Diagnosis Suggest ive Feat ures*
COPD Onset in mid-life.
Symptoms slowly progressive.
Long smoking history.
Dyspnea during exercise.
Largely irreversible airflow limitation.
Asthma Onset early in life (often childhood).
Symptoms vary from day to day.
Symptoms at night/early morning.
Allergy, rhinitis, and/or eczema also present.
Family history of asthma.
Largely reversible airflow limitation.
Congestive Heart Failure Fine basilar crackles on auscultation.
Chest X-ray shows dilated heart, pulmonary edema.
Pulmonary function tests indicate volume restriction, not airflow
limitation.
Bronchiectasis Large volumes of purulent sputum.
Commonly associated with bacterial infection.
Coarse crackles/clubbing on auscultation.
Chest X-ray/CT shows bronchial dilation, bronchial wall thickening.
Tuberculosis Onset all ages.
Chest X-ray shows lung infiltrate or nodular lesions.
Microbiological confirmation.
High local prevalence of tuberculosis.
Obliterative Bronchiolitis Onset in younger age, nonsmokers.
May have history of rheumatoid arthritis or fume exposure.
CT on expiration shows hypodense areas.
Diffuse Panbronchiolitis Most patients are male and nonsmokers.
Almost all have chronic sinusitis.
Chest X-ray and HRCT show diffuse small centrilobular
nodular opacities and hyperinflation.
Figu r e 3: Dif f er ent ial Diagnos is of COPD
*These features tend to be characteristic of the respective diseases, but do not occur in
every case. For example, a person who has never smoked may develop COPD (especially
in the developing world, where other risk factors may be more important than cigarette
smoking); asthma may develop in adult and even elderly patients.
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COMPONENTS OF CARE:
A COPD MANAGEMENT
PROGRAM
The goals of COPD management include:
Relieve symptoms
Prevent disease progression
Improve exercise tolerance
Improve health status
Prevent and treat complications
Prevent and treat exacerbations
Reduce mortality
Prevent or minimize side effects from treatment
Cessation of cigarette smoking should be included as a goal throughout
the management program.
THESE GOAL S CAN BE ACHI EVED THROUGH
I MPL EMENTATI ON OF A COPD MANAGEMENT P ROGRAM
WI TH FOUR COMPONENTS:
1. As sess and Monit or Dis eas e
2. Reduce Ris k Fact or s
3. Manage St abl e COPD
4. Manage Ex acer bat ions
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Component 1: Assess and Monitor Disease
A det ail ed medical his t or y of a new patient known or thought to
have COPD should assess:
Exposure to risk factors, including intensity and duration.
Past medical history, including asthma, allergy, sinusitis or nasal
polyps, respiratory infections in childhood, and other respiratory
diseases.
Family history of COPD or other chronic respiratory disease.
Pattern of symptom development.
History of exacerbations or previous hospitalizations for
respiratory disorder.
Presence of comorbidities, such as heart disease, malignancies,
osteoporosis, and musculoskeletal disorders, which may also
contribute to restriction of activity.
Appropriateness of current medical treatments.
Impact of disease on patients life, including limitation of activity;
missed work and economic impact; effect on family routines; and
feelings of depression or anxiety.
Social and family support available to the patient.
Possibilities for reducing risk factors, especially smoking cessation.
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In addition to s piromet r y, the following ot her t es t s may be considered
for the assessment of a patient with Moderate (Stage II), Severe
(Stage III), and Very Severe (Stage IV) COPD.
Bronchodil at or r ev er s ibil it y t est ing: To rule out a diagnosis of
asthma, particularly in patients with an atypical history (e.g., asthma
in childhood and regular night waking with cough and wheeze).
Ches t X - r ay : Seldom diagnostic in COPD but valuable to exclude
alternative diagnoses such as pulmonary tuberculosis, and identify
comorbidities such as cardiac failure.
Ar t er ial bl ood gas m easur ement : Perform in patients with
FEV
1
< 50% predicted or with clinical signs suggestive of respiratory
failure or right heart failure. The major clinical sign of respiratory
failure is cyanosis. Clinical signs of right heart failure include ankle
edema and an increase in the jugular venous pressure. Respiratory
failure is indicated by PaO
2
< 8.0 kPa (60 mm Hg), with or without
PaCO
2
> 6.7 kPa (50 mm Hg) while breathing air at sea level.
Al pha- 1 ant it r y psin def iciency scr eening: Perform when
COPD develops in patients of Caucasian descent under 45 years or
with a strong family history of COPD.
COP D is u su al l y a progr ess iv e disease. L u ng f unct ion
can be ex pect ed t o w or sen ov er t ime, ev en w it h t he best
av ail abl e car e. Sy mpt oms and l ung f u nct ion s hou l d be
monit or ed t o f ol l ow t he dev el opment of com pl icat ions , t o
gu ide t r eat ment , and t o f acil it at e dis cu ss ion of m anagem ent
opt ions wit h pat ient s . Comor bidit ies ar e comm on in COP D
and s hou l d be act iv el y ident if ied.
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Component 2: Reduce Risk Factors
Sm ok ing cess at ion is t he singl e m os t ef f ect iv eand cost -
ef f ect iveint er v ent ion t o r educe t he r is k of dev el oping
COP D and sl ow it s pr ogr ess ion.
Even a brief, 3-minute period of counseling to urge a smoker to
quit can be effective, and at a minimum this should be done for
every smoker at every health care provider visit. More intensive
strategies increase the likelihood of sustained quitting (Figur e 4).
Pharmacotherapy (nicotine replacement, buproprion/nortryptiline,
and/or varenicline) is recommended when counseling is not sufficient
to help patients stop smoking. Special consideration should be
given before using pharmacotherapy in people smoking fewer than
10 cigarettes per day, pregnant women, adolescents, and those
with medical contraindications (unstable coronary artery disease,
untreated peptic ulcer, and recent myocardial infarction or stroke
for nicotine replacement; and history of seizures for buproprion).
Figur e 4: St r at egy t o Hel p a Pat ient Quit Sm ok ing
1. ASK: Systematically identify all tobacco users at every visit.
Implement an office-wide system that ensures that, for EVERY patient
at EVERY clinic visit, tobacco-use status is queried and documented.
2. ADVI SE: Strongly urge all tobacco users to quit.
In a clear, strong, and personalized manner, urge every tobacco user
to quit.
3. ASSESS: Determine willingness to make a quit attempt.
Ask every tobacco user if he or she is willing to make a quit attempt
at this time (e.g., within the next 30 days).
4. ASSIST: Aid the patient in quitting.
Help the patient with a quit plan; provide practical counseling;
provide intra-treatment social support; help the patient obtain
extra-treatment social support; recommend use of approved
pharmacotherapy if appropriate; provide supplementary materials.
5. ARRANGE: Schedule follow-up contact.
Schedule follow-up contact, either in person or via telephone.
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Sm ok ing P r ev ent ion: Encourage comprehensive tobacco-control
policies and programs with clear, consistent, and repeated nonsmoking
messages. Work with government officials to pass legislation to establish
smoke-free schools, public facilities, and work environments and
encourage patients to keep smoke-free homes.
Occupat ional Ex posu r es : Emphasize primary prevention, which
is best achieved by elimination or reduction of exposures to various
substances in the workplace. Secondary prevention, achieved through
surveillance and early detection, is also important.
I ndoor and Out door Air Pol l ut ion: Implement measures to reduce
or avoid indoor air pollution from biomass fuel, burned for cooking and
heating in poorly ventilated dwellings. Advise patients to monitor public
announcements of air quality and, depending on the severity of their
disease, avoid vigorous exercise outdoors or stay indoors altogether
during pollution episodes.
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Component 3: Manage Stable COPD
Managem ent of s t abl e COPD s houl d be guided by t he
f ol l ow ing gener al pr incipl es :
Determine disease severity on an individual basis by taking into
account the patients symptoms, airflow limitation, frequency and
severity of exacerbations, complications, respiratory failure,
comorbidities, and general health status.
Implement a stepwise treatment plan that reflects this assessment of
disease severity.
Choose treatments according to national and cultural preferences,
the patients skills and preferences, and the local availability of
medications.
P at ient edu cat ion can help improve skills, ability to cope with illness,
and health status. It is an effective way to accomplish smoking cessation,
initiate discussions and understanding of advance directives and end-of-
life issues, and improve responses to acute exacerbations.
P har macol ogic t r eat ment (Figu r e 5) can control and prevent
symptoms, reduce the frequency and severity of exacerbations, improve
health status, and improve exercise tolerance.
Br onchodil at or s: These medications are central to symptom
management in COPD.
Inhaled therapy is preferred.
Give as needed to relieve intermittent or worsening symptoms, and
on a regular basis to prevent or reduce persistent symptoms.
The choice between
2
-agonists, anticholinergics, methylxanthines,
and combination therapy depends on the availability of medications
and each patients individual response in terms of both symptom
relief and side effects.
Regular treatment with long-acting bronchodilators, including nebu-
lized formulations, is more effective and convenient than treatment
with short-acting bronchodilators.
Combining bronchodilators of different pharmacologic classes may
improve efficacy and decrease the risk of side effects compared to
increasing the dose of a single bronchodilator.
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Figure 5. Formulations and Typical Doses of COPD Medications*
Drug Inhaler
(g)
Solution for
Nebulizer
(mg/ml)
Oral Vials for
Injection
(mg)
Duration of
Action (hours)

2
-agonists
Short-acting
Fenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6
Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8
Salbutamol (albuterol) 100, 200 (MDI & DPI) 5 5mg (Pill), 0.024%(Syrup) 0.1, 0.5 4-6
Terbutaline 400, 500 (DPI) 2.5, 5 (Pill) 4-6
Long-acting
Formoterol 4.5-12 (MDI & DPI) 0.01 12+
Arformoterol 0.0075 12+
Indacaterol 150-300 (DPI) 24
Salmeterol 25-50 (MDI & DPI) 12+
Anticholinergics
Short-acting
Ipratropium bromide 20, 40 (MDI) 0.25-0.5 6-8
Oxitropium bromide 100 (MDI) 1.5 7-9
Long-acting
Tiotropium 18 (DPI), 5 (SMI) 24+
Combination short-acting
2
-agonists plus anticholinergic in one inhaler
Fenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8
Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 6-8
Methylxanthines
Aminophylline 200-600 mg (Pill) 240 mg Variable, up to 24
Theophylline (SR) 100-600 mg (Pill) Variable, up to 24
Inhaled glucocorticosteroids
Beclomethasone 50-400 (MDI & DPI) 0.2-0.4
Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5
Fluticasone propionate 50-500 (MDI & DPI)
Combination long-acting
2
-agonists plus glucocorticosteroids in one inhaler
Formoterol/Budesonide 4.5/160, 9/320 (DPI)
Salmeterol/Fluticasone
propionate
50/100, 250. 500 (DPI)
25/50, 125, 250 (MDI)

Systemic glucocorticosteroids
Prednisone 5-60 mg (Pill)
Methyl-prednisolone 4, 8, 16 mg (Pill)
Phosphodiesterase-4 inhibitors
Roflumilast 500 mcg (Pill) 24
MDI=metered dose inhaler; DPI=dry powder inhaler
*Not all formulations are available in all countries; in some countries, other formulations may be available.
Formoterol nebulized solution is based on the unit dose vial containing 20 gm in a volume of 2.0ml
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Inhaled Glucocorticosteroids: Regular treatment with inhaled
glucocorticosteroids does not modify the long-term decline in FEV
1
but
has been shown to reduce the frequency of exacerbations and thus
improve health status for symptomatic patients with an FEV
1
< 50%
predicted and repeated exacerbations (for example, 3 in the last three
years). The dose-response relationships and long-term safety of inhaled
glucocorticosteroids in COPD are not known. Treatment with inhaled glu-
cocorticosteroids increases the likelihood of pneumonia and does not
reduce overall mortality.
An inhaled glucocorticosteroid combined with a long-acting
2
-agonist is
more effective than the individual components in reducing exacerbations
and improving lung function and health status. Combination therapy
increases the likelihood of pneumonia and has no significant effects on
mortality. In patients with an FEV
1
less than 60%, pharmacotherapy with
long-acting
2
-agonist, inhaled glucocorticosteroid and its combination
decreases the rate of decline of lung function. Addition of a long-acting

2
-agonist/inhaled glucocorticosteroid to an anticholinergic (tiotropium)
appears to provide additional benefits.
Oral Glucocorticosteroids: Long-term treatment with oral glucocorticosteroids
is not recommended.
Vaccines: Influenza vaccines reduce serious illness and death in COPD
patients by 50%. Vaccines containing killed or live, inactivated viruses
are recommended, and should be given once each year. Pneumococcal
polysaccharide vaccine is recommended for COPD patients 65 years and
older, and has been shown to reduce community-acquired pneumonia in
those under age 65 with FEV
1
< 40% predicted.
Ant ibiot ics : Not recommended except for treatment of infectious
exacerbations and other bacterial infections.
Mucol y t ic (Mu cok inet ic, Mucor egul at or ) Agent s: Patients with
viscous sputum may benefit from mucolytics, but overall benefits are very
small. Use is not recommended.
Ant it us siv es: Regular use contraindicated in stable COPD.
19
Phosphodiesterase-4 inhibitors: In patients with Stage III: Severe COPD or
Stage IV: Very Severe COPD and a history of exacerbations and chronic
bronchitis, the phosphodiesterase-4 inhibitor, roflumilast, reduces exacerba-
tions treated with oral glucocorticosteroids. These effects are also seen
when roflumilast is added to long-acting bronchodilators; there are no
comparison studies with inhaled glucocorticosteroids.
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Ox y gen Ther apy : The long-term administration of oxygen (>15 hours
per day) to patients with chronic respiratory failure increases survival and
has a beneficial impact on pulmonary hemodynamics, hematologic
characteristics, exercise capacity, lung mechanics, and mental state.
Initiate oxygen therapy for patients with Stage IV: Very Severe COPD if:
PaO
2
is at or below 7.3 kPa (55 mm Hg) or SaO
2
is at or below
88%, with or without hypercapnia; or
PO
2
is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg)
or SaO
2
is 88%, if there is evidence of pulmonary hypertension,
peripheral edema suggesting congestive heart failure, or
polycythemia (hematocrit > 55%).
Sur gical Tr eat m ent s : Bullectomy and lung transplantation may be
considered in carefully selected patients with Stage IV: Very Severe
COPD. There is currently no sufficient evidence that would support the
widespread use of lung volume reduction surgery (LVRS).
Ther e is no convincing evidence t hat mechanical v ent ilat or y
suppor t has a rol e in t he rout ine management of st able COPD.
20
The goal of l ong- t er m ox y gen t her apy is t o incr ease t he bas e-
l ine P aO
2
at r est t o at l east 8.0 k Pa (60 m m Hg) at s ea l ev el ,
and/or pr odu ce SaO
2
at l east 90%, w hich w il l pr es er v e v it al
or gan f u nct ion by ensu r ing an adequ at e del iv er y of ox y gen.
Non- P har macol ogic Tr eat ment includes rehabilitation, oxygen
therapy, and surgical interventions.
Patients at all stages of disease benefit from exercise training programs,
The goals of pu l m onar y r ehabil it at ion ar e t o r educe s ym pt om s,
im pr ov e qu alit y of l if e, and incr ease par t icipat ion in ev er y day
act iv it ies .
Rehabilitation: Patients at all stages of disease benefit from exercise
training programs improvements in exercise tolerance and symptoms of
dyspnea and fatigue. Benefits can be sustained even after a single pulmo-
nary rehabilitation program. The minimum length of an effective rehabili-
tation program is 6 weeks; the longer the program continues, the more
effective the results. Benefit does wane after a rehabilitation program
ends, but if exercise training is maintained at home the patient's health
status remains above pre-rehabilitation levels.
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A summary of characteristics and recommended treatment at each stage
of COPD is shown in Figur e 6.
21
Figure 6: Therapy at Each Stage of COPD*
*Postbronchodilator FEV
1
is recommended for the diagnosis and
assessment of severity of COPD.
FEV
1
/FVC < 0.70
FEV
1
8 0% predicted

FEV
1
/FVC < 0.70
50% FEV
1
< 80%
predicted
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting bronchodilators
(when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term oxygen if
chronic respiratory
failure
Consider surgical
treatments

FEV
1
/FVC < 0.70
30% FEV
1
< 50%
predicted

FEV
1
/FVC < 0.70
FEV
1
< 30% predicted
or FEV
1
< 50%
predicted plus chronic
respiratory failure

I: Mild II: Moderate III: Severe IV: Very Severe

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Component 4: Manage Exacerbations
An exacerbation of COPD is defined as an ev ent in t he nat ur al
cou r se of t he dis ease char act er ized by a change in t he
pat ient s bas el ine dy spnea, cou gh, and/or spu t u m t hat is
bey ond nor m al day - t o- day v ar iat ions, is acut e in ons et ,
and may war r ant a change in r egul ar medicat ion in a
pat ient w it h under l y ing COPD.
The most common causes of an exacerbation are infection of the
tracheobronchial tree and air pollution, but the cause of about one-third
of severe exacerbations cannot be identified.
How t o As sess t he Sev er it y of an Ex acer bat ion
Arterial blood gas measurements (in hospital):
PaO
2
< 8.0 kPa (60 mm Hg) and/or SaO
2
< 90% with or without
PaCO
2
> 6.7 kPa, (50 mmHg) when breathing room air indicates
respiratory failure.
Moderate-to-severe acidosis (pH < 7.36) plus hypercapnia (PaCO
2
> 6-8 kPa, 45-60 mm Hg) in a patient with respiratory failure is an
indication for mechanical ventilation.
Chest X-ray: Chest radiographs (posterior/anterior plus lateral) identify
alternative diagnoses that can mimic the symptoms of an exacerbation.
ECG: Aids in the diagnosis of right ventricular hypertrophy, arrhythmias,
and ischemic episodes.
Other laboratory tests:
Sputum culture and antibiogram to identify infection if there is
no response to initial antibiotic treatment.
Biochemical tests to detect electrolyte disturbances, diabetes,
and poor nutrition.
Whole blood count can identify polycythemia or bleeding.
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Hom e Management
Bronchodil at or s: Increase dose and/or frequency of existing short-
acting bronchodilator therapy, preferably with
2
-agonists. If not already
used, add anticholinergics until symptoms improve.
Gl u cocor t icost er oids : If baseline FEV
1
< 50% predicted, add 30-40
mg oral prednisolone per day for 7-10 days to the bronchodilator regimen.
Budesonide alone may be an alternative to oral glucocorticosteroids in the
treatment of exacerbations and is associated with significant reduction
of complications.
Hos pit al Managem ent
Patients with the characteristics listed in Figur e 7 should be hospitalized.
Indications for referral and the management of exacerbations of COPD
in the hospital depend on local resources and the facilities of the local
hospital.
Ant ibiot ics: Antibiotics should be given to patients:
With the following three cardinal symptoms: increased dyspnea,
increased sputum volume, increased sputum purulence
With increased sputum purulence and one other cardinal symptom
Who require mechanical ventilation
23
Hom e Car e or Hospit al Car e f or End- St age COPD Pat ient s?
The r isk of dy ing f rom an ex acer bat ion of COP D is cl os el y r el at ed
t o t he dev elopment of r es pir at or y acidos is , t he pr esence of
s er iou s com or bidit ies, and t he need f or v ent il at or y su ppor t .
P at ient s l ack ing t hese f eat u r es ar e not at high r is k of dy ing, bu t
t hose wit h sev er e u nder ly ing COP D of t en r equir e hospit al izat ion
in any case. At t empt s at managing s uch pat ient s ent ir ely in t he
com mu nit y hav e m et w it h l im it ed su cces s, bu t r et u r ning t hem
t o t heir hom es w it h incr eased s ocial su ppor t and a s uper v is ed
m edical car e progr am af t er an init ial em er gency r oom as ses sm ent
has been m u ch m or e su ccessf u l . How ev er, det ail ed cos t - benef it
anal ys es of t hese approaches hav e not been r epor t ed.
Figur e 7: I ndicat ions f or Hospit al Admission f or Ex acerbat ions
Marked increase in intensity of
symptoms, such as sudden develop-
ment of resting dyspnea
Severe underlying COPD
Onset of new physical signs (e.g.,
cyanosis, peripheral edema)
Failure of exacerbation to respond
to initial medical management
Significant comorbidities
Frequent exacerbations
Newly occurring arrhythmias
Diagnostic uncertainty
Older age
Insufficient home support
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APPENDIX I:
SPIROMETRY FOR
DIAGNOSIS OF COPD
Spirometry is as important for the diagnosis of COPD as blood
pressure measurements are for the diagnosis of hypertension.
Spirometry should be available to all health care professionals.
What is Spir omet r y ?
Spirom et r y is a simple test to measure the amount of air a
person can breathe out, and the amount of time taken to do so.
A s pirom et er is a device used to measure how effectively, and
how quickly, the lungs can be emptied.
A s pirogr am is a volume-time curve.
Spirometry measurements used for diagnosis of COPD include
(see Figure 2, page 9):
FVC (Forced Vital Capacity): maximum volume of air that
can be exhaled during a forced maneuver.
FEV
1
(Forced Expired Volume in one second): volume expired in
the first second of maximal expiration after a maximal inspiration.
This is a measure of how quickly the lungs can be emptied.
FEV
1
/FVC: FEV
1
expressed as a percentage of the FVC,
gives a clinically useful index of airflow limitation.
The ratio FEV
1
/FVC is between 70% and 80% in normal adults; a
value less than 70% indicates airflow limitation and the possibility
of COPD.
FEV
1
is influenced by the age, sex, height and ethnicity, and is
best considered as a percentage of the predicted normal value.
There is a vast literature on normal values; those appropriate for
local populations should be used
1,2,3
.
24
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Why do Spir om et r y f or COP D?
Spirometry is needed to make a firm diagnosis of COPD.
Together with the presence of symptoms, spirometry helps stage
COPD severity and can be a guide to specific treatment steps.
A normal value for spirometry effectively excludes the diagnosis
of clinically relevant COPD.
The lower the percentage predicted FEV
1
, the worse the
subsequent prognosis.
FEV
1
declines over time and faster in COPD than in healthy
subjects. Spirometry can be used to monitor disease progres-
sion, but to be reliable the intervals between measurements must
be at least 12 months.
What You Need t o Per f or m Spir om et r y
Several types of spirometers are available:
relatively large bellows or rolling-seal spirometers (usually only
available in pulmonary function laboratories). Calibration
should be checked against a known volume e.g. from a 3-litre
syringe on a regular basis.
smaller hand-held devices, often with electronic calibration
systems.
A hard copy of the volume time plot is very useful to check
optimal performance and interpretation, and to exclude errors.
Most spirometers require electrical power to permit operation of
the motor and/or sensors. Some battery operated versions are
available that can dock with a computer to provide hard copy.
25
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I t is es s ent ial t o l ear n how y our m achine is cal ibr at ed
and w hen and how t o cl ean it .
How t o P er f or m Spir omet r y
Spirometry is best performed with the patient seated. Patients may
be anxious about performing the tests properly, and should be
reassured. Careful explanation of the test, accompanied by a
demonstration, is very useful. The patient should:
Breathe in fully.
Seal their lips around the mouthpiece.
Force the air out of the chest as hard and fast as they can
until their lungs are completely empty.
Breathe in again and relax.
Exhalation must continue until no more air can be exhaled, must
be at least 6 seconds, and can take up to 15 seconds or more.
Like any test, spirometry results will only be of value if the
expirations are performed satisfactorily and consistently. Both
FVC and FEV
1
should be the largest value obtained from any of
3 technically satisfactory curves and the FVC and FEV
1
values in
these three curves should vary by no more than 5% or 100 ml,
whichever is greater. The FEV
1
/FVC is calculated using the maxi-
mum FEV
1
and FVC from technically acceptable (not necessarily
the same) curves.
Those with chest pain or frequent cough may be unable to
perform a satisfactory test and this should be noted.
26
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Wher e t o f ind mor e det ailed inf or mat ion on
s pir omet r y
1. Amer ican Thor acic Societ y
http://www.thoracic.org/adobe/statements/spirometry1-30.pdf
2. Aus t r al ian/New Zeal and Thor acic Societ y
http://www.nationalasthma.org.au/publications/spiro/index.htm
3. Br it is h Thor acic Societ y
http://www.brit-thoracic.org.uk/copd/consortium.html
4. GOLD
A spirometry guide for general practitioners and a teaching slide
set is available:
http://www.goldcopd.org
27
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28
NOTES
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Visit the GOLD website at www.goldcopd.org
The Global Initiative for Chronic Obstructive Lung Disease
is supported by unrestricted educational grants from:
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